The aim of this proposal is to investigate the efferent and afferent mechanisms responsible for the exaggerated natriuresis which we have observed in the dog when vertebral arterial Na concentration is increased. We will evaluate the afferent mechanism by determining 1) whether the receptors are responding to Na concentration or to osmolaity, 2) whether changes in the composition of the CSF are involved, and 3) what area of the brain perfused by the vertebral arteries is acting as a receptor. We will evaluate the efferent mechanisms by determining if the renal response is dependent 1) on changes in renal or peripheral hemodynamics, 2) on changes in the renin-angiotensin-aldosterine axis or 3) on the renal nerves. This proposal is based on our own studies in which we were examining the possible involvement of the CNS in the regulation of sodium excretion, an area in which there is an increasing body of data indicating that the CNS is involved. Our basic approach is to increase and decrease the Na concentration of the vertebral arterial blood keeping peripheral sodium concentration constant and examining the change in urinary sodium excretion in both anesthetized dogs and, in the future, in conscious dogs. These studies will furnish important new data on the mechanisms involved in the control of Na balance and on how the CNS participates in this control.